-
- Olabisi Oluwabukola Coker
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Zhenwei Dai
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Yongzhan Nie
- State Key Laboratory of Cancer Biology, Xijing Hospital, Fourth Military Medical University, Xian, China
-
- Guijun Zhao
- Department of Gastroenterology and Hepatology, Inner Mongolia People’s Hospital, Hohhot, China
-
- Lei Cao
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Geicho Nakatsu
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- William KK Wu
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Sunny Hei Wong
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Zigui Chen
- Department of Microbiology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
-
- Joseph J Y Sung
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
-
- Jun Yu
- Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, China
書誌事項
- 公開日
- 2017-08-01
- DOI
-
- 10.1136/gutjnl-2017-314281
- 公開者
- BMJ
この論文をさがす
説明
<jats:sec> <jats:title>Objectives</jats:title> <jats:p>We aimed to characterise the microbial changes associated with histological stages of gastric tumourigenesis.</jats:p> </jats:sec> <jats:sec> <jats:title>Design</jats:title> <jats:p>We performed 16S rRNA gene analysis of gastric mucosal samples from 81 cases including superficial gastritis (SG), atrophic gastritis (AG), intestinal metaplasia (IM) and gastric cancer (GC) from Xi’an, China, to determine mucosal microbiome dysbiosis across stages of GC. We validated the results in mucosal samples of 126 cases from Inner Mongolia, China.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p> We observed significant mucosa microbial dysbiosis in IM and GC subjects, with significant enrichment of 21 and depletion of 10 bacterial taxa in GC compared with SG (q<0.05). Microbial network analysis showed increasing correlation strengths among them with disease progression (p<0.001). Five GC-enriched bacterial taxa whose species identifications correspond to <jats:italic>Peptostreptococcus stomatis</jats:italic> , <jats:italic>Streptococcus anginosus</jats:italic> , <jats:italic>Parvimonas micra</jats:italic> , <jats:italic>Slackia exigua</jats:italic> and <jats:italic>Dialister pneumosintes</jats:italic> had significant centralities in the GC ecological network (p<0.05) and classified GC from SG with an area under the receiver-operating curve (AUC) of 0.82. Moreover, stronger interactions among gastric microbes were observed in <jats:italic>Helicobacter pylori</jats:italic> -negative samples compared with <jats:italic>H. pylori</jats:italic> -positive samples in SG and IM. The fold changes of selected bacteria, and strengths of their interactions were successfully validated in the Inner Mongolian cohort, in which the five bacterial markers distinguished GC from SG with an AUC of 0.81. </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p> In addition to microbial compositional changes, we identified differences in bacterial interactions across stages of gastric carcinogenesis. The significant enrichments and network centralities suggest potentially important roles of <jats:italic>P. stomatis</jats:italic> , <jats:italic>D. pneumosintes</jats:italic> , <jats:italic>S. exigua</jats:italic> , <jats:italic>P. micra</jats:italic> and <jats:italic>S. anginosus</jats:italic> in GC progression. </jats:p> </jats:sec>
収録刊行物
-
- Gut
-
Gut 67 (6), 1024-1032, 2017-08-01
BMJ
